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In this paper we present a new method for deriving It\^{o} stochastic delay differential equations (SDDEs) from delayed chemical master equations (DCMEs). Considering alternative formulations of SDDEs that can be derived from the same DCME, we prove that they are equivalent both in distribution, and in sample paths they produce. This allows us to formulate an algorithmic approach to deriving equivalent It\^{o} SDDEs with a smaller number of noise variables, which increases the computational speed of simulating stochastic delayed systems. The new method is illustrated on a simple model of two interacting species, and it shows excellent agreement with the results of direct stochastic simulations, while also demonstrating a much superior speed of performance., Comment: 15 pages, 3 figures

In this paper, we analyse a recently proposed predator-prey model with ratio dependence and Holling type III functional response, with particular emphasis on the dynamics close to extinction. By using Briot-Bouquet transformation we transform the model into a system, where the extinction steady state is represented by up to three distinct steady states, whose existence is determined by the values of appropriate Lambert W functions. We investigate how stability of extinction and coexistence steady states is affected by the rate of predation, predator fecundity, and the parameter characterising the strength of functional response. The results suggest that the extinction steady state can be stable for sufficiently high predation rate and for sufficiently small predator fecundity. Moreover, in certain parameter regimes, a stable extinction steady state can coexist with a stable prey-only equilibrium or with a stable coexistence equilibrium, and it is rather the initial conditions that determine whether prey and predator populations will be maintained at some steady level, or both of them will become extinct. Another possibility is for coexistence steady state to be unstable, in which case sustained periodic oscillations around it are observed. Numerical simulations are performed to illustrate the behaviour for all dynamical regimes, and in each case a corresponding phase plane of the transformed system is presented to show a correspondence with stable and unstable extinction steady state., Comment: 14 pages, 5 figures

This paper investigates the dynamics of immune response and autoimmunity with particular emphasis on the role of regulatory T cells (Tregs), T cells with different activation thresholds, and cytokines in mediating T cell activity. Analysis of the steady states yields parameter regions corresponding to regimes of normal clearance of viral infection, chronic infection, or autoimmune behaviour, and the boundaries of stability and bifurcations of relevant steady states are found in terms of system parameters. Numerical simulations are performed to illustrate different dynamical scenarios, and to identify basins of attraction of different steady states and periodic solutions, highlighting the important role played by the initial conditions in determining the outcome of immune interactions., Comment: 26 pages, 10 figures, accepted for publication in Int. J. Bif. Chaos

The paper addresses the problem of calculating the noise-induced switching rates in systems with delay-distributed kernels and Gaussian noise. A general variational formulation for the switching rate is derived for any distribution kernel, and the obtained equations of motion and boundary conditions represent the most probable, or optimal, path, which maximizes the probability of escape. Explicit analytical results for the switching rates for small mean time delays are obtained for the uniform and bi-modal (or two-peak) distributions. They suggest that increasing the width of the distribution leads to an increase in the switching times even for longer values of mean time delays for both examples of the distribution kernel, and the increase is higher in the case of the two-peak distribution. Analytical predictions are compared to the direct numerical simulations, and show excellent agreement between theory and numerical experiment., Comment: 21 oages and 4 figures

A major contribution to the onset and development of autoimmune disease is known to come from infections. An important practical problem is identifying the precise mechanism by which the breakdown of immune tolerance as a result of immune response to infection leads to autoimmunity. In this paper, we develop a mathematical model of immune response to a viral infection, which includes T cells with different activation thresholds, regulatory T cells (Tregs), and~a cytokine mediating immune dynamics. Particular emphasis is made on the role of time delays associated with the processes of infection and mounting the immune response. Stability analysis of various steady states of the model allows us to identify parameter regions associated with different types of immune behaviour, such as, normal clearance of infection, chronic infection, and autoimmune dynamics. Numerical simulations are used to illustrate different dynamical regimes, and to identify basins of attraction of different dynamical states. An important result of the analysis is that not only the parameters of the system, but also the initial level of infection and the initial state of the immune system determine the progress and outcome of the dynamics., Comment: 25 pages, 8 figures

Among various possible causes of autoimmune disease, an important role is played by infections that can result in a breakdown of immune tolerance, primarily through the mechanism of "molecular mimicry". In this paper we propose and analyse a stochastic model of immune response to a viral infection and subsequent autoimmunity, with account for the populations of T cells with different activation thresholds, regulatory T cells, and cytokines. We show analytically and numerically how stochasticity can result in sustained oscillations around deterministically stable steady states, and we also investigate stochastic dynamics in the regime of bi-stability. These results provide a possible explanation for experimentally observed variations in the progression of autoimmune disease. Computations of the variance of stochastic fluctuations provide practically important insights into how the size of these fluctuations depends on various biological parameters, and this also gives a headway for comparison with experimental data on variation in the observed numbers of T cells and organ cells affected by infection., Comment: 27 pages, 5 figures

A new detailed mathematical model for dynamics of immune response to hepatitis B is proposed, which takes into account contributions from innate and adaptive immune responses, as well as cytokines. Stability analysis of different steady states is performed to identify parameter regions where the model exhibits clearance of infection, maintenance of a chronic infection, or periodic oscillations. Effects of nucleoside analogues and interferon treatments are analysed, and the critical drug efficiency is determined., Comment: 24 pages, 10 figures

This paper investigates the effects of vaccination on the dynamics of infectious disease, which is spreading in a population concurrently with awareness. The model considers contributions to the overall awareness from a global information campaign, direct contacts between unaware and aware individuals, and reported cases of infection. It is assumed that there is some time delay between individuals becoming aware and modifying their behaviour. Vaccination is administered to newborns, as well as to aware individuals, and it is further assumed that vaccine-induced immunity may wane with time. Feasibility and stability of the disease-free and endemic equilibria are studied analytically, and conditions for the Hopf bifurcation of the endemic steady state are found in terms of system parameters and the time delay. Analytical results are supported by numerical continuation of the Hopf bifurcation and numerical simulations of the model to illustrate different types of dynamical behaviour., Comment: 18 pages, 4 figures

We consider a globally coupled network of active (oscillatory) and inactive (non-oscillatory) oscillators with distributed-delay coupling. Conditions for aging transition, associated with suppression of oscillations, are derived for uniform and gamma delay distributions in terms of coupling parameters and the proportion of inactive oscillators. The results suggest that for the uniform distribution increasing the width of distribution for the same mean delay allows aging transition to happen for a smaller coupling strength and a smaller proportion of inactive elements. For gamma distribution with sufficiently large mean time delay, it may be possible to achieve aging transition for an arbitrary proportion of inactive oscillators, as long as the coupling strength lies in a certain range., Comment: 21 pages, 7 figures

This paper analyses the dynamics of infectious disease with a concurrent spread of disease awareness. The model includes local awareness due to contacts with aware individuals, as well as global awareness due to reported cases of infection and awareness campaigns. We investigate the effects of time delay in response of unaware individuals to available information on the epidemic dynamics by establishing conditions for the Hopf bifurcation of the endemic steady state of the model. Analytical results are supported by numerical bifurcation analysis and simulations., Comment: 15 pages, 5 figures

This paper analyses an SIRS-type model for infectious diseases with account for behavioural changes associated with the simultaneous spread of awareness in the population. Two types of awareness are included into the model: private awareness associated with direct contacts between unaware and aware populations, and public information campaign. Stability analysis of different steady states in the model provides information about potential spread of disease in a population, and well as about how the disease dynamics is affected by the two types of awareness. Numerical simulations are performed to illustrate the behaviour of the system in different dynamical regimes., Comment: 18 pages, 7 figures

Cross-protection, which refers to a process whereby artificially inoculating a plant with a mild strain provides protection against a more aggressive isolate of the virus, is known to be an effective tool of disease control in plants. In this paper we derive and analyse a new mathematical model of the interactions between two competing viruses with particular account for RNA interference. Our results show that co-infection of the host can either increase or decrease the potency of individual infections depending on the levels of cross-protection or cross-enhancement between different viruses. Analytical and numerical bifurcation analyses are employed to investigate the stability of all steady states of the model in order to identify parameter regions where the system exhibits synergistic or antagonistic behaviour between viral strains, as well as different types of host recovery. We show that not only viral attributes but also the propagating component of RNA-interference in plants can play an important role in determining the dynamics., Comment: 28 pages, 7 figures

RNA interference (RNAi) is a fundamental cellular process that inhibits gene expression through cleavage and destruction of target mRNA. It is responsible for a number of important intracellular functions, from being the first line of immune defence against pathogens to regulating development and morphogenesis. In this paper we consider a mathematical model of RNAi with particular emphasis on time delays associated with two aspects of primed amplification: binding of siRNA to aberrant RNA, and binding of siRNA to mRNA, both of which result in the expanded production of dsRNA responsible for RNA silencing. Analytical and numerical stability analyses are performed to identify regions of stability of different steady states and to determine conditions on parameters that lead to instability. Our results suggest that while the original model without time delays exhibits a bi-stability due to the presence of a hysteresis loop, under the influence of time delays, one of the two steady states with the high (default) or small (silenced) concentration of mRNA can actually lose its stability via a Hopf bifurcation. This leads to the co-existence of a stable steady state and a stable periodic orbit, which has a profound effect on the dynamics of the system., Comment: 31 pages, 11 figures, accepted for publication to Ecological Complexity

In the studies of plant infections, the plant immune response is known to play an essential role. In this paper we derive and analyse a new mathematical model of plant immune response with particular account for post-transcriptional gene silencing (PTGS). Besides biologically accurate representation of the PTGS dynamics, the model explicitly includes two time delays to represent the maturation time of the growing plant tissue and the non-instantaneous nature of the PTGS. Through analytical and numerical analysis of stability of the steady states of the model we identify parameter regions associated with recovery and resistant phenotypes, as well as possible chronic infections. Dynamics of the system in these regimes is illustrated by numerical simulations of the model., Comment: 26 pages, 7 figures

In this review we discuss different mathematical models of gene regulatory networks as relevant to the onset and development of cancer. After discussion of alternative modelling approaches, we use a paradigmatic two-gene network to focus on the role played by time delays in the dynamics of gene regulatory networks. We contrast the dynamics of the reduced model arising in the limit of fast mRNA dynamics with that of the full model. The review concludes with the discussion of some open problems., Comment: 27 pages, 6 figures

This paper studies the stability of synchronized states in networks where couplings between nodes are characterized by some distributed time delay, and develops a generalized master stability function approach. Using a generic example of Stuart-Landau oscillators, it is shown how the stability of synchronized solutions in networks with distributed delay coupling can be determined through a semi-analytic computation of Floquet exponents. The analysis of stability of fully synchronized and of cluster or splay states is illustrated for several practically important choices of delay distributions and network topologies., Comment: 18 pages, 4 figures

We show that oscillation death as a specific type of oscillation suppression, which implies symmetry breaking, can be controlled by introducing time-delayed coupling. In particular, we demonstrate that time delay influences the stability of an inhomogeneous steady state, providing the opportunity to modulate the threshold for oscillation death. Additionally, we find a novel type of oscillation death representing a secondary bifurcation of an inhomogeneous steady state., Comment: 6 pages, 4 figures

Effects of immune delay on symmetric dynamics are investigated within a model of antigenic variation in malaria. Using isotypic decomposition of the phase space, stability problem is reduced to the analysis of a cubic transcendental equation for the eigenvalues. This allows one to identify periodic solutions with different symmetries arising at a Hopf bifurcation. In the case of small immune delay, the boundary of the Hopf bifurcation is found in a closed form in terms of system parameters. For arbitrary values of the time delay, general expressions for the critical time delay are found, which indicate bifurcation to an odd or even periodic solution. Numerical simulations of the full system are performed to illustrate different types of dynamical behaviour. The results of this analysis are quite generic and can be used to study within-host dynamics of many infectious diseases., Comment: 21 page, 4 figures. arXiv admin note: substantial text overlap with arXiv:1202.4290

This paper studies the effects of distributed delay coupling on the dynamics in a system of non-identical coupled Stuart-Landau oscillators. For uniform and gamma delay distribution kernels, conditions for amplitude death are obtained in terms of average frequency, frequency detuning and parameters of the coupling, including coupling strength and phase, as well as the mean time delay and the width of the delay distribution. To gain further insight into the dynamics inside amplitude death regions, eigenvalues of the corresponding characteristic equations are computed numerically. Oscillatory dynamics of the system is also investigated using amplitude and phase representation. Various branches of phase-locked solutions are identified, and their stability is analysed for different types of delay distributions., Comment: 25 pages, 13 figures

This paper studies the effects of coupling with distributed delay on the suppression of oscillations in a system of coupled Stuart-Landau oscillators. Conditions for amplitude death are obtained in terms of strength and phase of the coupling, as well as the mean time delay and the width of the delay distribution for uniform and gamma distributions. Analytical results are confirmed by numerical computation of the eigenvalues of the corresponding characteristic equations. These results indicate that larger widths of delay distribution increase the regions of amplitude death in the parameter space. In the case of a uniformly distributed delay kernel, for sufficiently large width of the delay distribution it is possible to achieve amplitude death for an arbitrary value of the average time delay, provided that the coupling strength has a value in the appropriate range. For a gamma distribution of delay, amplitude death is also possible for an arbitrary value of the average time delay, provided that it exceeds a certain value as determined by the coupling phase and the power law of the distribution. The coupling phase has a destabilizing effect and reduces the regions of amplitude death., Comment: 15 pages, 7 figures

This paper studies the effects of a time-delayed feedback control on the appearance and development of spatiotemporal patterns in a reaction-diffusion system. Different types of control schemes are investigated, including single-species, diagonal, and mixed control. This approach helps to unveil different dynamical regimes, which arise from chaotic state or from traveling waves. In the case of spatiotemporal chaos, the control can either stabilize uniform steady states or lead to bistability between a trivial steady state and a propagating traveling wave. Furthermore, when the basic state is a stable traveling pulse, the control is able to advance stationary Turing patterns or yield the above-mentioned bistability regime. In each case, the stability boundary is found in the parameter space of the control strength and the time delay, and numerical simulations suggest that diagonal control fails to control the spatiotemporal chaos., Comment: 14 pages, 8 figures

We present an analysis of time-delayed feedback control used to stabilize an unstable steady state of a neutral delay differential equation. Stability of the controlled system is addressed by studying the eigenvalue spectrum of a corresponding characteristic equation with two time delays. An analytic expression for the stabilizing control strength is derived in terms of original system parameters and the time delay of the control. Theoretical and numerical results show that the interplay between the control strength and two time delays provides a number of regions in the parameter space where the time-delayed feedback control can successfully stabilize an otherwise unstable steady state., Comment: 11 pages, 8 figures

Spectral properties and transition to instability in neutral delay differential equations are investigated in the limit of large delay. An approximation of the upper boundary of stability is found and compared to an analytically derived exact stability boundary. The approximate and exact stability borders agree quite well for the large time delay, and the inclusion of a time-delayed velocity feedback improves this agreement for small delays. Theoretical results are complemented by a numerically computed spectrum of the corresponding characteristic equations., Comment: 14 pages, 6 figures

An epidemic model with distributed time delay is derived to describe the dynamics of infectious diseases with varying immunity. It is shown that solutions are always positive, and the model has at most two steady states: disease-free and endemic. It is proved that the disease-free equilibrium is locally and globally asymptotically stable. When an endemic equilibrium exists, it is possible to analytically prove its local and global stability using Lyapunov functionals. Bifurcation analysis is performed using DDE-BIFTOOL and traceDDE to investigate different dynamical regimes in the model using numerical continuation for different values of system parameters and different integral kernels., Comment: 16 pages, 5 figures